期刊文献+

5-methoxytryptophan induced apoptosis and PI3K/Akt/FoxO3a phosphorylation in colorectal cancer 被引量:2

下载PDF
导出
摘要 BACKGROUND Colorectal cancer(CRC)is a highly prevalent malignancy worldwide,and new therapeutic targets urgently need to be found to prolong patient survival.5-methoxytryptophan(5-MTP)is a tryptophan metabolite found in animals and humans.However,the effects of 5-MTP on proliferation and apoptosis of CRC cells are currently unknown.AIM To investigate the effects of 5-MTP on the proliferation,migration,invasion,and apoptosis abilities of CRC cells.Additionally,we seek to explore whether 5-MTP has the potential to be utilized as a drug for the treatment of CRC.METHODS In order to evaluate the effect of 5-MTP on CRC cells,a series of experiments were conducted for evaluation.Colony formation assay and Cell Counting Kit 8 assays were used to investigate the impact of 5-MTP on the proliferation of CRC cell lines.Cell cycle assays were employed to examine the effect of 5-MTP on cellular growth.In addition,we investigated the effects of 5-MTP on apoptosis and reactive oxygen species in HCT-116 cells.To obtain a deeper understanding of how 5-MTP affects CRC,we conducted a study to examine its influence on the PI3K/Akt signaling pathway in CRC cells.RESULTS This article showed that 5-MTP promoted apoptosis and cell cycle arrest and inhibited cell proliferation in CRC cells.In many articles,it has been reported that PI3K/Akt/FoxO3a signaling pathway is one of the most important signaling pathways involved in internal regulating cell proliferation and differentiation. Nevertheless, 5-MTP combined with PI3K/Akt/FoxO3a signaling pathway inhibitors significantly promotedapoptosis and cell cycle arrest and inhibited cell proliferation in CRC cells compared with 5-MTP alone in ourstudy.CONCLUSIONTherefore, there is strong evidence that 5-MTP can be used as an effective medicine for CRC treatment.
出处 《World Journal of Gastroenterology》 SCIE CAS 2023年第47期6148-6160,共13页 世界胃肠病学杂志(英文版)
  • 相关文献

参考文献3

二级参考文献3

共引文献127

同被引文献27

引证文献2

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部